A couple of your symtoms could be related to environmental
pollutants.

- osteoarthritic knees / aching joints [see abstract below]
- eroding teeth at base [see abstract below]

- night sweat
- white furring of the tongue
- nighttime urination

Positive associations of serum concentration of polychlorinated
biphenyls or organochlorine pesticides with self-reported arthritis,
especially rheumatoid type, in women.
BACKGROUND: Persistent organic pollutants (POPs) can influence the
immune system, possibly increasing the risk of rheumatoid arthritis
(RA). In addition, as metabolic change due to obesity has been
proposed as one mechanism of osteoarthritis (OA), POPs stored in
adipose tissue may be also associated with OA. OBJECTIVE: Our goal in
this study was to examine associations of background exposure to POPs
with arthritis among the general population. DESIGN: We investigated
cross-sectional associations of serum POPs concentrations with the
prevalence of self-reported arthritis in 1,721 adults >/= 20 years of
age in the National Health and Nutrition Examination Survey 1999-2002.
RESULTS: Among several POPs, dioxin-like polychlorinated biphenyls
(PCBs) or nondioxin-like PCBs were positively associated with
arthritis in women. After adjusting for possible confounders, odds
ratios (ORs) were 1.0, 2.1, 3.5, and 2.9 across quartiles of dioxin-
like PCBs (p for trend = 0.02). Corresponding figures for nondioxin-
like PCBs were 1.0, 1.6, 2.6, and 2.5 (p for trend = 0.02).
Organochlorine (OC) pesticides were also weakly associated with
arthritis in women. For subtypes of arthritis, respectively, RA was
more strongly associated with PCBs than was OA. The adjusted ORs for
RA were 1.0, 7.6, 6.1, and 8.5 for dioxin-like PCBs (p for trend =
0.05), 1.0, 2.2, 4.4, and 5.4 for nondioxin-like PCBs (p for trend <
0.01), and 1.0, 2.8, 2.7, and 3.5 for OC pesticides (p for trend =
0.15). POPs in men did not show any clear relation with arthritis.
CONCLUSIONS: The possibility that background exposure to PCBs may be
involved in pathogenesis of arthritis, especially RA, in women should
be investigated in prospective studies. PMID: 17589595

Developmental dental toxicity of dioxin and related compounds--a
review.
Non-halogenated polycyclic aromatic hydrocarbons (PAHs) and
halogenated aromatic hydrocarbons such as polychlorinated dibenzo-p-
dioxins and dibenzofurans (PCDD/Fs, or dioxins), and polychlorinated
biphenyls (PCBs) are wide-spread environmental pollutants that have
unequivocal adverse effects on different species, including humans.
Accidental exposure of children to high amounts of PCDD/Fs has been
found to be associated with developmental enamel defects and missing
permanent teeth. An association between dioxin exposure via mother's
milk and developmental mineralisation defects in permanent first
molars was also found in otherwise healthy Finnish children born in
the late 1980s but not in those born in the late 1990s. Results of
experimental animal studies in vivo and in vitro are compatible with
findings in human teeth. In addition to the dose, dental effects of
the most toxic dioxin congener, 2,3,7,8-tetrachlorodibenzo-p-dioxin
(TCDD), essentially depend on the stage of tooth development at the
time of exposure. Accordingly, TCDD arrests early rat and mouse molar
tooth development and in more advanced teeth it interferes with
mineralisation of enamel and dentine and arrests root development.
Expression of the specific dioxin receptor (AhR) in dental cells at
TCDD-sensitive stages of tooth development suggests that the dental,
like other developmental effects of TCDD, are mediated by the AhR.
Early effects also depend on the epidermal growth factor receptor and
involve enhanced apoptosis. The lowest TCDD dose (30ng/kg) causing
adverse dental effects in rats has been estimated to result in
maternal tissue levels approaching the high end of human background
range and human milk PCDD/F levels that were associated with enamel
defects in children. However, because of the uniform and clear decline
in background dioxin and PCB levels in mother's milk during the last
twenty years, dioxins are currently likely to be of small or no
account as regards developmental dental defects in children. Even so,
this is not the case after heavy exposure and little is known about
the possible synergistic effects of these toxicants with other
chemicals interfering with tooth development. PMID: 17243464

Inhibition of dioxin effects on bone formation in vitro by a newly
described aryl hydrocarbon receptor antagonist, resveratrol.
Aryl hydrocarbon receptor (AhR) ligands are environmental contaminants
found in cigarette smoke and other sources of air pollution. The
prototypical compound is TCDD (2,3,7, 8-tetrachlorodibenzo-p-dioxin),
also known as dioxin. There is an increasing body of knowledge linking
cigarette smoking to osteoporosis and periodontal disease, but the
direct effects of smoke-associated aryl hydrocarbons on bone are not
well understood. Through the use of resveratrol (3,5,4'-
trihydroxystilbene), a plant antifungal compound that we have recently
demonstrated to be a pure AhR antagonist, we have investigated the
effects of TCDD on osteogenesis. It was postulated that TCDD would
inhibit osteogenesis in bone-forming cultures and that this inhibition
would be antagonized by resveratrol. We employed the chicken
periosteal osteogenesis (CPO) model, which has been shown to form bone
in vitro in a pattern morphologically and biochemically similar to
that seen in vivo, as well as a rat stromal cell bone nodule formation
model. In the CPO model, alkaline phosphatase (AP) activity was
reduced by up to 50% (P<0.01 vs control) in the presence of 10(-9) M
TCDD and these effects were reversed by 10(-6) M resveratrol (P<0.05
vs TCDD alone). TCDD-mediated inhibition of osteogenesis was
restricted primarily to the osteoblastic differentiation phase (days
0-2) as later addition did not appear to have any effects. Message
levels for important bone-associated proteins (in the CPO model) such
as collagen type I, osteopontin, bone sialoprotein and AP were
inhibited by TCDD, an effect that was antagonized by resveratrol.
Similar findings were obtained using the rat stromal bone cell line.
TCDD (at concentrations as low as 10(-10)M) caused an approximately
33% reduction in AP activity, which was abrogated by 3. 5x10(-7) M
resveratrol. TCDD also induced a marked reduction in mineralization
( approximately 75%) which was completely antagonized by resveratrol.
These data suggest that AhR ligands inhibit osteogenesis probably
through inhibition of osteodifferentiation and that this effect can be
antagonized by resveratrol. Since high levels of AhR ligands are found
in cigarette smoke, and further since smoking is an important risk
factor in both osteoporosis and periodontal disease, it may be
postulated that AhR ligands are the component of cigarette smoke
linking smoking to osteoporosis and periodontal disease. If so,
resveratrol could prove to be a promising preventive or therapeutic
agent for smoking-related bone loss. PMID: 11018766